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PubMed1996

Regulation of vascular smooth muscle contraction. The roles of Ca2+, protein kinase C and myosin light chain phosphatase.

Vasoconstrictors bind to their receptors on the cell surface to active phospholipase C and Ca2+ channels, resulting in the mobilization of Ca2+ from intracellular are extracellular Ca2+ pools and protein kinase C activation. Vasoconstrictors are also thought to activate a distinct cellular mechanism for downregulating 20 kDa myosin light chain (MLC20) phosphatase activity, which involves Rho p21 and protein kinase C, resulting in an increase in the Ca2+ sensitivity of MLC20 phosphorylation. Protein kinase C also appears to activate a MLC20 phosphorylation-independent mechanism for contraction, contributing to the maintenance of agonist-induced contraction. On the other hand, vasorelaxants inhibit activation of phospholipase C and gating of Ca2+ channels, or stimulate Ca2+ extrusion across the plasma membrane, leading to a decrease in the [Ca2+]i. Vasorelaxants also appear to stimulate MLC20 phosphatase activity, resulting in a further reduction of contractile response. The modulatory mechanism for changing the Ca2+ sensitivity, together with the major regulatory mechanism for cellular Ca2+ metabolism, plays an important role in regulating vascular smooth muscle tone.

Animals↗
PubMed1999

Dynamic measurement of myosin light-chain-domain tilt and twist in muscle contraction.

A new method is described for measuring motions of protein domains in their native environment on the physiological timescale. Pairs of cysteines are introduced into the domain at sites chosen from its static structure and are crosslinked by a bifunctional rhodamine. Domain orientation in a reconstituted macromolecular complex is determined by combining fluorescence polarization data from a small number of such labelled cysteine pairs. This approach bridges the gap between in vitro studies of protein structure and cellular studies of protein function and is used here to measure the tilt and twist of the myosin light-chain domain with respect to actin filaments in single muscle cells. The results reveal the structural basis for the lever-arm action of the light-chain domain of the myosin motor during force generation in muscle.

Animals↗
PubMed1983

Acetylcholine and an unidentified, muscle-contracting factor in the venom of the bumblebee, Bombus terrestris L.

Extracts of venom reservoirs as well as dilutions of venom droplets collected from the tip of the sting of Bombus terrestris were tested for biological activity on the isolated guinea-pig ileum, the frog rectus abdominis, and the rat phrenic nerve-hemidiaphragm preparation. The venom contains a cholinergic factor, apparently identical to acetylcholine, at a concentration of about 30 micrograms per venom reservoir. This was confirmed using radioimmunoassay of acetylcholine. The venom also contains a component causing a slow contraction of guinea-pig ileum and rat diaphragm. This component is heat stable, non dialysable, and is slowly destroyed in the venom preparation at about 0 degrees C.

Acetylcholine↗
PubMed1989

[Objective assessment and quantification of postmortem muscle contraction to electrical stimulation].

UNLABELLED: The muscular contraction on electrical stimulation (rectangular impulses of 1 s duration, 2 to 80 mA current intensity) was objectified using a sensitive force transducer. RESULTS: The shape of the muscular contraction (time course) is changing over the postmortem interval with two peaks (opening and closing contraction according to Pflüger's law) in the early postmortem interval and only one peak in the later postmortem interval. The relaxation period of muscular contraction is increasing over the postmortem interval. The maximum force developed during muscular contraction on definite current intensity is decreasing over the postmortem interval. Increase of the relaxation period a decrease of the maximum force in response to a definite current intensity are criteria allowing a determination of the time since death on an objective basis.

Electric Stimulation↗
PubMed2004

Recent X-ray diffraction studies of muscle contraction and their implications.

Recent studies on the interference fringes in the myosin meridional reflections provide a new source of structural information on cross-bridge movement during mechanical transients and steady shortening. Many observations can be interpreted satisfactorily by the tilting lever-arm model, with some assumptions, including the presence of fixed repeating structures contributing to the M3 and higher-order meridional reflections. In isometric contraction, the lever arms are oriented near the start of the working stroke, with a dispersion of ca+/-20-25 degrees . Upon a rapid release of 10-12 nm, they move to the end of the stroke, with a well-known T2 delay of 1-2 ms. This delay must represent additional processes, which have to occur even in tension-generating heads, or activation of attached heads, which initially do not develop force. Surprisingly, in muscles shortening at moderate loads (0.5-0.6 P0), the mean position of the heads moves only 2-3 nm closer to the M-line than in the isometric case, reminiscent of the Piazzesi-Lombardi model.

Animals↗
PubMed1991

Vascular smooth muscle contraction induced by Na+ channel activators, veratridine and batrachotoxin.

The effects of the sodium channel activators veratridine and batrachotoxin on isolated rat aorta were investigated. Veratridine caused gradual contraction, independent of the presence of endothelium, with an EC50 of 35 microM. Batrachotoxin (1 microM) also induced contraction. Both effects were completely inhibited by the sodium channel blocker tetrodotoxin (1 microM). The veratridine (60 microM)-induced contraction was inhibited by nifedipine (0.1 microM). In the absence of extracellular Ca2+, veratridine (60 microM) did not cause contraction. Sodium nitroprusside (80 nM), acetylcholine (10 microM) and isoproterenol (1 microM) caused relaxation of rings precontracted with veratridine (60 microM). An inhibitor of endothelium-derived relaxing factor (EDRF) synthase, N omega-nitro-L-arginine methyl ester (L-NAME) (0.65 mM), enhanced the veratridine-induced contraction in rings with an intact endothelium, which suggests that EDRF was being released during the veratridine-induced contraction. These results show that the activation of sodium channels on smooth muscle cells induces a contraction that is probably mediated by Ca2+ influx through voltage-dependent Ca2+ channels.

Animals↗
PubMed1986

Role of tropomyosin in smooth muscle contraction: effect of tropomyosin binding to actin on actin activation of myosin ATPase.

The binding of gizzard tropomyosin to gizzard F-actin is highly dependent on free Mg2+ concentration. At 2 mM free Mg2+, a concentration at which actin-activated ATPase activity was shown to be Ca2+ sensitive, a molar ratio of 1:3 (tropomyosin:actin monomer) is required to saturate the F-actin with tropomyosin to the stoichiometric ratio of 1 mol of tropomyosin to 7 mol of actin monomer. Increasing the Mg2+ could decrease the amount of tropomyosin required for saturating the F-actin filament to the stoichiometric level. Analysis of the binding of smooth muscle tropomyosin to smooth muscle actin by the use of Scatchard plots indicates that the binding exhibits strong positive cooperativity at all Mg2+ concentrations. Calcium has no effect on the binding of tropomyosin to actin, irrespective of the free Mg2+ concentration. However, maximal activation of the smooth muscle actomyosin ATPase in low free Mg2+ requires the presence of Ca2+ and stoichiometric binding of tropomyosin to actin. The lack of effect of Ca2+ on the binding of tropomyosin to actin shows that the activation of actomyosin ATPase by Ca2+ in the presence of tropomyosin is not due to a calcium-mediated binding of tropomyosin to actin.

Actins↗
PubMed1994

Effects of aqueous extracts of six marine microalgae on smooth muscle contraction in rat duodenum and vas deferens.

We report the effects of aqueous extracts of six marine microalgae on responses to various contractile agents in isolated rat duodenum (acetylcholine, calcium chloride, barium chloride) and vas deferens (noradrenaline). Our results suggest that only extracts of Phaeodactylum tricornutum, Skeletonema costatum, and Chlorella stigmatophora may have pharmacological potential. Extracts of these three species had spasmolytic effects on responses to the three contractile agents in duodenum. In vas deferens, P. tricornutum and C. stigmatophora inhibited the contractions induced by noradrenaline, whilst S. costatum showed a non-dose-dependent potentiation. With the aim of elucidating their mechanisms of action, we are attempting to isolate the active principles present in these extracts.

Animals↗
PubMed2001

Efffect of noscapine, the antitussive opioid alkaloid, on bradykinin-induced smooth muscle contraction in the isolated ileum of the guinea-pig.

Bradykinin (BK) and related kinins are autocoid peptides that play integral roles in many pathophysiological processes such as cough. In this study, the inhibitory effect of noscapine, the antitussive opioid alkaloid, on BK receptors, was tested in the guinea-pig ileum. Contractions of the isolated ileum of the guinea-pig in response to BK were inhibited by noscapine (10-1,000 nM) in a concentration-dependent manner. Concentration-response curves (CRCs) to BK were slightly shifted to the right with a concomitant decrease in the maximum effect. A pA2 value of 6.68 was calculated for noscapine. The slope of the Schild plot of the antagonism was found to be 0.56. Noscapine had no effect on contractions induced by KCl, acetylcholine, histamine, 5-hydroxy tryptamine or angiotensin II. In conclusion, noscapine has a specific antagonistic effect on BK receptors and the mode of inhibition was found to be non-competitive.

Animals↗
PubMed1997

Change in urethral pressure during voluntary pelvic floor muscle contraction and vaginal electrical stimulation.

The purpose of the study was to compare the effect of voluntary pelvic floor muscle (FFM) contraction and vaginal electrical stimulation on urethral pressure. Twelve women with genuine stress incontinence, mean age 49.4 years (range 33-66) participated in the study. The urethral and bladder pressures were recorded simultaneously through a double-lumen 8 Ch catheter. The patients first performed three voluntary PFM contractions. Then two electrical stimulators, Conmax and Medicon MS 105, 50 Hz, were used in random order. A visual analog scale was used to measure pain and discomfort. Pain was reported to mean 6.8, SEM 0.64 (range 0.7-9.9) and mean 6.1, SEM 0.81 (range 0-9.1) with Conmax and Medicon MS 105, respectively. The mean paired difference in favor of voluntary contraction with Conmax was -8.0, SD 6.7, P = 0.0067, and with Medicon MS 105 it was -12.2, SD 5.9, P = 0.0022. The results demonstrated that voluntary PFM contraction increased urethral pressure significantly more than did vaginal electrical stimulation.

Adult↗
PubMed2001

Mast cell-independent impairment of host defense and muscle contraction in T. spiralis-infected W/W(V) mice.

In response to nematode infection, the host presumably attempts to create an unfavorable environment to prevent larval penetration of the host and to expedite parasite expulsion from the gut. In this study, we have used W/W(V) mice with or without mast cells after bone marrow reconstitution (BMR-W/W(V)) to examine the role of mast cells in the host response. W/W(V), BMR-W/W(V), and wild-type (+/+) mice were infected with Trichinella spiralis. Infected W/W(V) mice exhibited less tissue damage and experienced a delay in worm expulsion and a greater degree of larval penetration of the gut leading to encystment in skeletal muscle. Tissue injury was greater and worm expulsion was normalized in BMR-W/W(V) mice, but larval penetration remained unchanged. Spontaneous contractile activity of jejunal muscle was disrupted in W/W(V) mice, as was the contractile response to carbachol. These abnormalities were also present in BMR-W/W(V) mice. These results indicate that mast cells mediate tissue damage and contribute to the timely expulsion of nematodes from the gut during primary infection.

Animals↗
PubMed2005

Emotion and movement: activation of defensive circuitry alters the magnitude of a sustained muscle contraction.

Understanding the emotion-movement relationship is crucial to the development of motor theory and movement rehabilitation recommendations for a wide range of diseases and injuries that involve motor impairment. Behaviorally, when movements are executed following exposure to emotional stimuli, evidence suggests that active defensive circuitry results in faster but more variable voluntary movements. However, each of the existing protocols has involved movement execution following the offset of anxiety or emotion eliciting stimuli. The specific aim of this study, therefore, was to determine whether the continued exposure to emotional stimuli would alter the magnitude and variability of a sustained motor contraction. During the presentation of pleasant, unpleasant, neutral, and blank images, participants (N=45) were instructed to respond to the onset of an auditory stimulus by initiating and then sustaining a maximal bimanual isometric contraction of the wrist and finger extensor muscles against two independent load cells (left/right limb). Corroborating previous evidence and supporting hypothesis 1, findings indicated that exposure to unpleasant images lead to an increase in mean force production. Variability of movement, however, did not vary as a function of affective context. These findings indicate that continued exposure to unpleasant stimuli magnifies the force production of a sustained voluntary movement, without sacrificing the variability of that contraction. Mechanism driven open and closed loop explanations are offered for these phenomena, implications are addressed, and future directions are discussed.

Adolescent↗
PubMed1976

Coronary arterial smooth muscle contraction by a substance released from platelets: evidence that it is thromboxane A2.

When human platelets are aggregated by thrombin, material is released that rapidly contracts strips of spirally cut porcine coronary artery. Prevention of the contraction by indomethacin suggested mediation by a prostaglandin. The contraction produced by aggregating platelets was unlike those produced by prostaglandins E2, F2alpha, G2, or H2, but resembled that evoked by thromboxane A2, which is formed by platelets during aggregation.

Arteries↗
PubMed1990

On the down-regulation of cross-bridges occurring as changes in the cycling rate during tonic smooth muscle contractions.

As regards cross-bridge down-regulation, the following statements may summarize the results of our experiments: 1) The time course of cross-bridge down-regulation is the initial high turn-over rate followed by a continuous retardation without any distinct loss in force generation. These mechanisms allowed a rapid force development and an improvement in force maintenance. 2) Cross-bridge down-regulation was seen in the tracheal preparation of both the rat and the guinea pig. As indicated by the greater time constants of the post-vibration force recovery, the cross-bridge cycling rate seems to be distinctly lower in the guinea pig than in the rat trachea. 3) Cross-bridge down-regulation only occurs in smooth muscle preparations with intact cell membranes. This result would seem to hint that the sarcoplasmatic calcium concentration and/or the intactness of the cell membrane might be essential for producing cross-bridge down-regulation. 4) The recovery from cross-bridge down-regulation requires a rest period of more than 10s. The cross-bridges remain down-regulated during this time even after an increase in the sarcoplasmatic calcium concentration which was induced by a subsequent stimulus. This result indicates that changes in the sarcoplasmatic calcium cannot explain all the problems arising during cross-bridge down-regulation.

Acetylcholine↗
PubMed1980

Mechanisms of ouabain-induced arterial muscle contraction.

Ouabain caused dose-related contractions in helically cut strips of cerebral, mesenteric, renal, and femoral arteries isolated from dogs and monkeys; the contractions were elicited at lower concentrations in cerebral than in the peripheral arteries. Contractions induced by ouabain were abolished by exposure of cerebral arteries to Ca2+-free media. Contractions induced by Ca2+ in Ca2+-free media were potentiated by ouabain. Substitution of LiCl for NaCl and reduction of [K+]0 suppressed the contractile response of cerebral arteries to ouabain. Pretreatment of dogs with reserpine abolished the response of peripheral arteries to ouabain but not the cerebroarterial response. Phentolamine also abolished the response of peripheral arteries. Once oubain-induced contractions were stabilized, the alpha-antagonist caused a marked relaxation in peripheral but not in cerebral arteries. Ouabain-induced contractions appear to be mediated by an increase in the Ca2+ influx that results mainly from an inhibition of the electrogenic Na+ pump in low concentrations (cerebral arteries) and from a release of norepinephrine from nerves in high concentrations (mesenteric, renal, and femoral arteries).

Animals↗
PubMed1992

Smooth muscle contraction bands in intestinal infarction.

We studied microscopic sections of 24 cases of intestinal infarction looking for contraction bands (CB) in the muscularis propria of the bowel wall. Controls were 11 surgical and 11 autopsy cases from patients who did not suffer any form of ischaemic disease. The difference of CB frequency was significant (P less than 0.001) in infarction versus the surgical control group. Moreover, within the study group the CB frequency was also related to the severity of the ischaemic lesion (P less than 0.01). With immunostaining, CB were not reactive with antibodies against vimentin, desmin, actin or myosin. We propose that CB genesis in intestinal smooth muscle is related to hypoxia, possibly through altered homeostasis of calcium and catecholamine metabolism.

Aged↗
PubMed1972

An energetic model of muscle contraction.

Initial energy utilization in the twitch is visualized as the result of the activity of two distinct processes. The first is the calcium-pumping activity of the sarcoplasmic reticulum, which has a constant energy requirement under normal conditions. The second is the chemomechanical transduction process consisting of a variable number of quantal contractile events, each with a fixed enthalpy equal to the molecular enthalpy of adenosine triphosphate (ATP) hydrolysis in vivo. This enthalpy appears either as heat or as contractile element work. Total enthalpy varies according to the number of quantal contractile events that occur in the twitch cycle. The basis of the variation is suggested to be velocity-dependent activity of the actomyosin ATPase, allowing more quantal events to occur in a contraction cycle when shortening occurs. The classical designation "activation heat" is held to be appropriate for the first process. The partition of the enthalpy of the second process that is currently in vogue is held to be misleading and a new formulation is suggested in which the properties of the quantal contractile event are reflected in general terms. The formulation of the proposed transduction model represents a conceptual return to the viscoelastic theory, but at a quantal level. The model can explain the results of the preceding paper and is adaptable to different muscles without having to postulate fundamental differences in energy utilization.

Actomyosin↗